The purpose of this study is to determine if lack of glucagon suppression causes postprandial hyperglycemia in the presence of impaired insulin secretion in subjects with type 2 diabetes mellitus. Eight subjects with type 2 diabetes mellitus have been studied on two occasions. On both occasions volunteers received a 50g glucose drink while their endogenous hormone production was inhibited by somatostatin. Insulin was infused to mimic a diabetic postprandial profile. Glucagon was infused at a rate of 1.25 ng/kg/min beginning either at time zero to prevent a fall in postprandial glucagon concentrations or beginning at two hours so as to create a transient fall in plasma glucagon concentrations. Studies conducted up till now indicate that the non-suppressibility of glucagon does not contribute significantly to high blood glucose after meal when insulin secretion is impaired in people with type 2 diabetes mellitus. We observed an unforeseen fall in the insulin concentrations immediately after oral glucose ingestion. This was due to a "standard basal insulin infusion" with somatostatin starting at time zero. We propose to avoid this by modifying the experiment. The unwanted fall of insulin levels can be avoided by determining individual "basal" insulin requirements. Somatostatin will be started at time -240. Insulin infusion will continue to be adjusted to maintain overnight euglycemia in the same insulin infusion rate will continue throught the study. For this modification, we have taken approval from IRB (1/12/99) and Radiation Safety to study volunteers four (rather than the approved three) times. We do not anticipate a need to go beyond the approved number of volunteers and the four studies per volunteer to finish the study. We plan to continue studying the volunteers and finish the study by the end of 2000.